{"id":"dac209434cad","type":"article","url":"https://hartvaat.nl/2018/07/10/residueel-inflammatoir-risico-bij-pcsk9-remming-plus-statine/","title":"Residueel inflammatoir risico bij PCSK9-remming plus statine","title_en":"Residual Inflammatory Risk on Treatment With PCSK9 Inhibition and Statin Therapy.","category":"cholesterol","category_label":"Cholesterol","professions":["cardioloog","internist"],"tags":["enlicitide","ezetimibe","ldl-cholesterol","niet-statine-therapie","pcsk9-remmers","pcsk9-remmers-nieuwe-generatie","rosuvastatine","statines"],"journal":"Circulation","doi":"10.1161/CIRCULATIONAHA.118.034645","source_url":"https://doi.org/10.1161/CIRCULATIONAHA.118.034645","authors":["Aruna D Pradhan","Aaron W Aday","Lynda M Rose","Paul M Ridker"],"significance":8,"published":"2018-07-10","source_date":"2018-07-10","image":"","kennis":["https://hartvaat.nl/kennis/lipiden/lipidenmedicatie-bij-ckd/","https://hartvaat.nl/kennis/lipiden/residueel-cardiovasculair-risico/"],"congress":"","summary_en":"This study quantified the residual inflammatory risk that persists after maximum LDL cholesterol lowering with PCSK9 inhibition and statins, demonstrating that elevated hsCRP remains an independent predictor of events even at very low LDL levels. The results provided the rationale for adding anti-inflammatory therapy to lipid-lowering strategies.","created":"2026-07-03T10:27:21Z","updated":"2026-07-03T13:26:36Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Studie naar het residuele inflammatoire risico dat overblijft na maximale LDL-verlaging met PCSK9-remming en statines. Kwantificeert het 'inflammation gap'.","abstract_original":"BACKGROUND: The combination of statin therapy and PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition markedly lowers low-density lipoprotein cholesterol (LDL-C) and reduces cardiovascular event rates. Whether residual inflammatory risk as measured by on-treatment high sensitivity C-reactive protein (hsCRP) remains an important clinical issue in such patients is uncertain. METHODS: We evaluated residual inflammatory risk among 9738 patients participating in the SPIRE-1 and SPIRE-2 cardiovascular outcomes trials (Studies of PCSK9 Inhibition and the Reduction in Vascular Events), who were receiving both statin therapy and bococizumab, according to on-treatment levels of hsCRP (hsCRPOT) and LDL-COT measured 14 weeks after drug initiation. The primary end point was nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina requiring urgent revascularization, or cardiovascular death. RESULTS: At 14 weeks, the mean percentage change in LDL-C among statin-treated patients who additionally received bococizumab was -60.5% (95% confidence interval [CI], -61.2 to -59.8; P<0.001; median change, -65.4%) as compared to 6.6% (95% CI, -1.0 to 14.1; P=0.09; median change, 0.0%) for hsCRP. Incidence rates for future cardiovascular events for patients treated with both statin therapy and bococizumab according to hsCRPOT <1, 1 to 3, and >3 mg/L were 1.96, 2.50, and 3.59 events per 100 person-years, respectively, corresponding to multivariable adjusted hazard ratios of 1.0, 1.16 (95% CI, 0.81-1.66), and 1.62 (95% CI, 1.14-2.30) (P-trend=0.001) after adjustment for traditional cardiovascular risk factors and LDL-COT. Comparable adjusted hazard ratios for LDL-COT (<30, 30-50, >50 mg/dL) were 1.0, 0.87, and 1.21, respectively (P-trend=0.16). Relative risk reductions with bococizumab were similar across hsCRPOT groups (P-interaction=0.87). CONCLUSIONS: In this post hoc analysis of the SPIRE trials of bococizumab in a stable outpatient population, evidence of residual inflammatory risk persisted among patients treated with both statin therapy and proprotein convertase subtilisin-kexin type 9 inhibition. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifiers: NCT01975376, NCT01975389."}